Cecilie Petterson Oksvold

• Liao, Yiliu; Kristiansen, Åse-Marit; Oksvold, Cecilie Petterson; Tuvnes, Frode Alexander; Gu, Ning & Rundén-Pran, Elise [Show all 9 contributors for this article] (2010). Neuronal Ca2+-Activated K+ Channels Limit Brain Infarction and Promote Survival. PLOS ONE. 5(12). doi: 10.1371/journal.pone.0015601. Full text in Research Archive Show summary

  Neuronal calcium-activated potassium channels of the BK type are activated by membrane depolarization and intracellular Ca2+ ions. It has been suggested that these channels may play a key neuroprotective role during and after brain ischemia, but this hypothesis has so far not been tested by selective BK-channel manipulations in vivo. To elucidate the in vivo contribution of neuronal BK channels in acute focal cerebral ischemia, we performed middle cerebral artery occlusion (MCAO) in mice lacking BK channels (homozygous mice lacking the BK channel alpha subunit, BK−/−). MCAO was performed in BK−/− and WT mice for 90 minutes followed by a 7-hour-reperfusion period. Coronal 1 mm thick sections were stained with 2,3,5-triphenyltetrazolium chloride to reveal the infarction area. We found that transient focal cerebral ischemia by MCAO produced larger infarct volume, more severe neurological deficits, and higher post-ischemic mortality in BK−/− mice compared to WT littermates. However, the regional cerebral blood flow was not significantly different between genotypes as measured by Laser Doppler (LD) flowmetry pre-ischemically, intra-ischemically, and post-ischemically, suggesting that the different impact of MCAO in BK−/− vs. WT was not due to vascular BK channels. Furthermore, when NMDA was injected intracerebrally in non-ischemic mice, NMDA-induced neurotoxicity was found to be larger in BK−/− mice compared to WT. Whole-cell patch clamp recordings from CA1 pyramidal cells in organotypic hippocampal slice cultures revealed that BK channels contribute to rapid action potential repolarization, as previously found in acute slices. When these cultures were exposed to ischemia-like conditions this induced significantly more neuronal death in BK−/− than in WT cultures. These results indicate that neuronal BK channels are important for protection against ischemic brain damage.

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• Tuvnes, Frode Alexander; Storm, Johan Frederik; Larsson, Pål Gunnar; Mateos-Aparicio, Pedro; Murphy, Ricardo & Oksvold, Cecilie Petterson [Show all 8 contributors for this article] (2013). Hva skjer i hjernen din? Full text in Research Archive Show summary

  Hva skjer i hjernen din? Hva er hukommelse? Hva er bevissthet? Hva skjer i hjernen din når du føler noe? Hvordan kan elektriske impulser kode tanker? Hos oss kan du: - Se hjernebølger. - Se levende hjernevev og hjerneceller. - Se og høre hjernecellene sende signaler til hverandre. - Se matematiske modeller av hjernecellenes signaler. Akkurat nå, mens du leser denne teksten, farer milliarder av elektriske signaler gjennom cellene i hjernen din. Men hva er egentlig disse gåtefulle hjerneprosessene? Vår forskergruppe prøver å finne svarene. Kom og få et innbilkk i hva som foregår i hjernen din!

• Liao, Yiliu; Kristiansen, Åse-Marit; Oksvold, Cecilie Petterson; Tuvnes, Frode Alexander; Gu, Ning & Rundén-Pran, E. [Show all 9 contributors for this article] (2009). Neuronal Ca2+-activated K+ channels limit brain infarction and promote survival. Full text in Research Archive
• Stranden, Einar; Oksvold, Cecilie Petterson & Morken, Brit (1998). 6. Skin flowmotion in simulated hypovolemia. Journal of Vascular Research. ISSN 1018-1172. 35(4), p. 299–299. Full text in Research Archive
• Oksvold, Cecilie Petterson (1996). Studier av flowmosjon i hud hos mennesker: effekt av eksterne stimuli. Universitetet i Oslo. Full text in Research Archive

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